Burning Muscle Pain

In the list of symptoms I have approximate 10 specific and different muscle pains described. They are each connected to a separate combination of nutrients, possibly even with different layers of healing despite being all in the muscles. One of them specifically is what feels like lactic acid burn that went on for 17 years for me. This is of specific interest in Salt Lake since our resident FMS/CFS researchers, Drs Light (both of them). As they work up at the U of U my pain docs follow their work carefully. One of the things that they are involved with is what causes that pain and how to get rid of it. In my discussion with my doc we discussed the role of exercise and lack there of. It appears that the burn sensors proliferate during non use of muscles, the inactivity forced on all of us. I wonder if there is a failure of mitochondria to proliferate when these sensors do proliferate? They sure seem to go together. For me, the pain faded, but that wasn't sufficient for exercise tolerance to return. That took both AdoCbl and LCF to restore the tolerance to exercise to then rebuild the mitochondria and muscles.

My experiences was that the burning pain of 17 years duration actually decreased to almost zero in 10 days following the start of MeCbl and the return of some energy. However, it took AdoCbl and LCF to restore exercise tolerance, mitochondria proliferation and muscle growth. He was interested in how I went from essentially housebound and able to do a few steps up the stairs at a time to being able to do 2000-4000 feet of vertical up AND down each day with 3 to 5 miles or more of walking distance, at least during the summer. The doc I started with at the pain clinic had retired from the clinic so I was reassigned and he hadn't watched from the beginning. I had 99% of my total healing while still having paradoxical folate insufficiency symptoms. These slowly squeezed down to a very few "signal" symptoms. While keeping these minimized, at least other layers of healing can be going on.

As usual, this doc watches and agrees that I am doing well and that treatment should continue. I sure don't look like or have affect like the rest of the patients there. The thing about the pain clinic which they tell us up front is that they are not there for finding a cure to our problems. They are there to manage the pain that in itself has become the problem, regardless of underlying problems.

With most of my nerves functioning adequately to have nerves to muscles, most of my muscles have come back except for those having nerves that were damaged by the car wreck, showing the asymmetries quite strongly.

I don't know that it does or doesn't have anything to do with it EMFs. Whatever the cause it has been around apparently unchanged for 60 + years. Also my maternal grandfather had the same problems for 50 years before I was even born. Neurological pain will return if the vitamins are discontinued for several reasons. One doc with experience at healing neuropathy said it takes 5 years of uninterrupted b12 etc to permanently heal the nerves. If it can't be healed 100% it appears to require b12 for the rest of the life to maintain benefit. Nerve damage is very difficult to fully heal. The neurological pain I had following the car wreck went away and seems permanently gone. It didn't come back when the CNS problems did with the two crashes.

To me, methylators are speaking a different language and this thread is no different. I need a translation. I assume MeCbl is methylcobalamin, but what are AdoCbl and LCF? Can you provide a link that explains methylation is simple english? I would like to learn more about it, but need a place to start. Thanks.

According to Dr Jack Kruse, the problems with EMFs go back many decades when homes were getting electricity, artificial light, radios, TVs and so on. Technology has been growing exponentially along with disease since then.

To me, methylators are speaking a different language and this thread is no different. I need a translation. I assume MeCbl is methylcobalamin, but what are AdoCbl and LCF? Can you provide a link that explains methylation is simple english? I would like to learn more about it, but need a place to start. Thanks.

LCF is involved in energy metabolism and protection of nerve cells from damage by sugar via the polyol pathway.
(Don't know anything about the polyol pathway but it is the name of the pathway should you desire to research it...gotta have the right buzz word to effectively search).

*NOTE: Life Extension (and heartfixer and possibly enzymestuff) take the view that most people do not need active forms of the B vitamins...they feel that genetic defects are rare and the only reason to require active B's. We, here, know that is not true. Unfortunately there is no source of info that necessarily possesses the whole truth in the matter. You have to read with your own critical reasoning skills and make your own decisions. Although the info on the above sites is consolidated and well written and an easy IN to understaning methtylation, phoeniz rising has more information on it than any of the above sources.

http://www.lef.org/magazine/mag2000/may00-cover2.htmThe Antiaging Effects of Acetyl-L-Carnitine ...By facilitating the youthful transport of fatty acids into the cell's mitochondria, acetyl-L-carnitine better enables dietary fats to be converted to energy and muscle. Carnitine is approved as a drug in the United States to protect against muscle wasting diseases, including heart muscle weakness and low energy levels....

Velha recovered from CFS using Freddd's protocol and 4-5g/day of LCF (She said only 2 brands were potent, Drs Best and some other I cannot recall). The article above shows benefits from ALC, but the only CFS benefit I have heard was from LCF. I suspect the overlap somewhat in benefits, but LCF is clearly the one you want if you reached this site.

http://www.lef.org/protocols/abstracts/abstr-082.htmlPolyol pathway hyperactivity is closely related to carnitine deficiency in the pathogenesis of diabetic neuropathy of streptozotocin-diabetic rats.
Nakamura J, Koh N, Sakakibara F, Hamada Y, Hara T, Sasaki H, Chaya S, Komori T, Nakashima E, Naruse K, Kato K, Takeuchi N, Kasuya Y, Hotta N. The Third Department of Internal Medicine, Nagoya University School of Medicine, Nagoya, Japan.
J Pharmacol Exp Ther 1998 Dec;287(3):897-902
To investigate the relationship between polyol pathway hyperactivity and altered carnitine metabolism in the pathogenesis of diabetic neuropathy, the effects of an aldose reductase inhibitor, [5-(3-thienyl) tetrazol-1-yl]acetic acid (TAT), and a carnitine analog, acetyl-L-carnitine (ALC), on neural functions and biochemistry and hemodynamic factors were compared in streptozotocin-diabetic rats. Significantly delayed motor nerve conduction velocity, decreased R-R interval variation, reduced sciatic nerve blood flow and decreased erythrocyte 2, 3-diphosphoglycerate concentrations in diabetic rats were all ameliorated by treatment with TAT (administered with rat chow containing 0.05% TAT, approximately 50 mg/kg/day) or ALC (by gavage, 300 mg/kg/day) for 4 weeks. Platelet hyperaggregation activity in diabetic rats was diminished by TAT but not by ALC. TAT decreased sorbitol accumulation and prevented not only myo-inositol depletion but also free-carnitine deficiency in diabetic nerves. On the other hand, ALC also increased the myo-inositol as well as the free-carnitine content without affecting the sorbitol content. These observations suggest that there is a close relationship between increased polyol pathway activity and carnitine deficiency in the development of diabetic neuropathy and that an aldose reductase inhibitor, TAT, and a carnitine analog, ALC, have therapeutic potential for the treatment of diabetic neuropathy.

In the list of symptoms I have approximate 10 specific and different muscle pains described. They are each connected to a separate combination of nutrients, possibly even with different layers of healing despite being all in the muscles. One of them specifically is what feels like lactic acid burn that went on for 17 years for me. This is of specific interest in Salt Lake since our resident FMS/CFS researchers, Drs Light (both of them). As they work up at the U of U my pain docs follow their work carefully. One of the things that they are involved with is what causes that pain and how to get rid of it. In my discussion with my doc we discussed the role of exercise and lack there of. It appears that the burn sensors proliferate during non use of muscles, the inactivity forced on all of us. I wonder if there is a failure of mitochondria to proliferate when these sensors do proliferate? They sure seem to go together. For me, the pain faded, but that wasn't sufficient for exercise tolerance to return. That took both AdoCbl and LCF to restore the tolerance to exercise to then rebuild the mitochondria and muscles.

My experiences was that the burning pain of 17 years duration actually decreased to almost zero in 10 days following the start of MeCbl and the return of some energy. However, it took AdoCbl and LCF to restore exercise tolerance, mitochondria proliferation and muscle growth. He was interested in how I went from essentially housebound and able to do a few steps up the stairs at a time to being able to do 2000-4000 feet of vertical up AND down each day with 3 to 5 miles or more of walking distance, at least during the summer. The doc I started with at the pain clinic had retired from the clinic so I was reassigned and he hadn't watched from the beginning. I had 99% of my total healing while still having paradoxical folate insufficiency symptoms. These slowly squeezed down to a very few "signal" symptoms. While keeping these minimized, at least other layers of healing can be going on.

As usual, this doc watches and agrees that I am doing well and that treatment should continue. I sure don't look like or have affect like the rest of the patients there. The thing about the pain clinic which they tell us up front is that they are not there for finding a cure to our problems. They are there to manage the pain that in itself has become the problem, regardless of underlying problems.

With most of my nerves functioning adequately to have nerves to muscles, most of my muscles have come back except for those having nerves that were damaged by the car wreck, showing the asymmetries quite strongly.

Click to expand...

I've been experiencing burning (warmer than expected) feet lately. Is this a folate issue so I should increase it. I'm @ 3mg mB12 8.6mg cB12 2,000 mcg folate....do I hear a 2,400????? On another NOTE:
I had lactic acid BURN in my shins after doing a marathon (shopping trip that is) in NYC for Thanksgiving. I suffered for 3 weeks saying, "oh it's shin splints" Took some Potassium and I was good to go.... This coudn't be potassium again????

As regards the warm feeling of feet with these nutrients it is a change that happens at certain "stages". Sometimes things are getting better and sometimes worse. However, when it is a response to these nutrients it is favorable generally and all stages are gone through in reverse order. If it is going in the right direction then changes slowly happen towards feeling more normal. So my feet may burn with neurology but I haven't had any lactic acid burn on a prolonged basis in 10 years. I don't overdo exercise. That is individual because most all summer I'll be walking 3-5 miles a day and 2000 feet of vertical up and down, but I don't jog and push the speed to the edge as I used to until the muscle pain became too much. Moving my pace from 5 miles in 45 minutes to 5 miles in 40 minutes took considerable effort. I don't jog anymore, too much strain on the joints. I work up to things at a speed that doesn't make me sore.

The chronic lactic acid type burn lasted 17 years in all the muscles in my body. Just hold up my head and body was enough to do it.